Micro/nanorobots have the potential to be remotely propelled and manipulated in complex biological fluid and organ tissue. However, the combination of the sophisticated physiological barriers, remote‐controlled navigation, real‐time motion tracking, and diagnostic/therapeutic effects are tremendous challenges for application and translation. An unique sequential magneto‐actuated and optics‐triggered biomicrorobot (AI microrobot) for actively targeted cancer treatment is prepared. The AI microrobot consists of two components, magnetospirillum magneticum (AMB‐1), providing the ability to autonomously swim toward the tumor site via internal hypoxia‐driven effects and an external applied magnetic field, and indocyanine green nanoparticles, acting as a fluorescence imaging agent and photothermal therapy. The AI microrobots are tracked in vivo by fluorescence and magnetic resonance imaging. It is found that the AI microrobots can sequentially migrate to the hypoxic internal area of tumors and then effectively eradicate solid tumors through photothermal therapy under NIR laser irradiation. The sequential magneto‐actuated and optics‐triggered AI microrobots platform described here presents a bioinspired strategy toward remotely controlled propulsion, actively targeted cargo delivery, and satisfactory therapeutic performance in the circulatory system.

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The mechanism responsible for the apoptotic effect induced by ent-11α-hydroxy-15-oxo-kaur-16-en-19-oic-acid (5F) is not fully understood and its in vivo effect has not been tested. In this study, the effect and mechanism of 5F was investigated in cigarette smoking carcinogen 4-methylnitrosamino-1-3-pyridyl-butanone (NNK)-induced mouse lung tumor model and in cultured lung cancer cells NCI-H23 and CRL-2066. 5F were given to mice after they were treated with NNK for 18 weeks. The effect of 5F on the lung tumor formation was examined, and its side effect was monitored. Cell proliferation and apoptosis were determined through expression of PCNA, Bcl-2, Bax, and TUNEL assay in in vivo animal model. 5F significantly inhibited the NNK-induced lung tumors by inducing apoptosis and suppressing cell proliferation in vivo with minimal side effects. Cell culture experiments showed that 5F translocated Bax into the mitochondria, downregulated Bcl-2, activated caspase-9 and caspase-3, released cytochrome c into the cytosol, and translocated AIF from the mitochondria to the nucleus, which leading to G2-M cell cycle arrest and cell apoptosis. 5F also activated ERK1/2 and the inhibition of ERK1/2 suppressed 5F-mediated changes in apoptotic molecules. In addition to ERK1/2, 5F activated Akt. The inhibition of Akt further facilitated the apoptosis induced, suggesting that Akt activation was anti-apoptotic rather than pro-apoptotic. Collectively, 5F is effective against lung cancer in vivo with minimal side effects. It induces apoptosis in lung cancer through the mitochondrial-mediated pathway, in which the activation of ERK is critical.